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First published online May 1, 2006
doi: 10.1242/10.1242/dev.02359

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Signs of change: hormone receptors that regulate plant development

Anthony Bishopp^1,*, Ari Pekka Mähönen^1,* and Ykä Helariutta^1,2,3,

¹ Plant Molecular Biology Laboratory, Institute of Biotechnology, POB 56, FI-00014, University of Helsinki, Finland.
² Department of Biology, FI-20014, University of Turku, Finland.
³ Umeå Plant Science Centre, Department of Forest Genetics and Plant Physiology, Swedish University of Agricultural Sciences, SE-901 83, Umeå, Sweden.

View larger version (26K): [in a new window]   Fig. 1. Auxin and gibberellin signalling pathways. (A) Under low auxin concentrations, the transcription of auxin-response genes via the ARFs is blocked by the Aux/IAA transcriptional repressor proteins. (B) In Arabidopsis, auxin is bound by the F-box protein TIR1, or by other AFB proteins that comprise the SCFTIR1 complex (RBX1-Cullin-ASK1-TIR1 in the figure). The binding of auxin stimulates the interaction of Aux/IAAs with SCFTIR1 and so promotes the ubiquitination of Aux/IAAs proteins, targeting them for destruction by the 26S proteosome and releasing the ARFs from their inhibitory chaperone proteins. (C,D) In rice, gibberellin (GA) signalling involves a similar process, whereby transcription of the gibberellin-response genes is regulated by the GA-dependent degradation of the DELLA protein SLR1. (C) Under low gibberellin concentrations, SLR1 represses gibberellin responses. (D) Under high gibberellin concentrations, GA binds to the GID1 protein directly and initiates a GA-dependent interaction with SLR1. The SCFGID2 complex is then recruited to ubiquitinate SLR1, leading to its degradation. It is unclear whether GID1-GA induces stable conformational changes to SLR1 that lead to the recruitment of the SCFGID2 complex, or whether the GA-GID1-SLR1 is targeted by SCFGID2 as a whole. GA-TF, gibberellin-dependent transcription factors; +mod, unknown modification; NM, nuclear membrane; OsCUL1, Oryza sativa Cullin homologue 1; OsSKP15, Oryza sativa ASK1 homologue 15; +ub, ubiquitination.

View larger version (101K): [in a new window]   Fig. 2. Phenotypes associated with the auxin and gibberellin receptor mutants. All images are shown alongside wild type for comparison. (A) A wild-type Arabidopsis plant (left) and a quadruple auxin receptor mutant, tir1 afb1 afb2 afb3, which has reduced apical dominance and size (right). (B). Cell division of the hypophysis (arrows), which is necessary for root meristem specification, is strongly delayed in tir1 afb2 afb3 globular embryos (right). (C) Growth of the rice gibberellin receptor mutant gid1-1 (right) is severely reduced. Inset: higher magnification of gid1-1. Scale bars, 10 cm (1 cm in inset). [A and B are reprinted, with permission, from Dharmasiri et al. (Dharmasiri et al., 2005b). C is reprinted, with permission, from Ueguchi-Tanaka et al. (Ueguchi-Tanaka et al., 2005).]

View larger version (19K): [in a new window]   Fig. 3. Composition of the transmembrane phytohormone receptors. (A) A diagram of the structure of brassinosteroid (BR) receptors. The number of leucine-rich repeats (LRR) is indicated. (B,C) Structure of ethylene (B) and (C) cytokinin receptors. These diagrams are not to scale.

View larger version (30K): [in a new window]   Fig. 4. Brassinosteroid signalling pathway. (A) In low brassinosteroid (BR) concentration, the BIN2 kinase rapidly phosphorylates the brassinosteroid-dependent transcriptional regulators, BES1 and BZR1, leading to their subsequent ubiquitination and degradation via the 26S proteasome. (B) When BR is perceived by the membrane-localised BRI1-BAK1 heterodimer, BIN2 is inhibited by an indirect, unknown mechanism. This leads to the accumulation of dephosphorylated BES1 and BZR1 in the nucleus, where they regulate the transcription of BR-regulated genes, either by transcriptional activation or inhibition. NM, nuclear membrane; +P, phosphorylation; PM, plasma membrane; +ub, ubiquitination.

View larger version (106K): [in a new window]   Fig. 5. Phenotypes associated with the brassinosteroid, ethylene, cytokinin and abscisic acid receptor mutants. All images are shown against wild type for comparison. (A) The brassinosteroid receptor mutant bri1-301 (bottom) shows a dwarf phenotype. (B) The dark-grown ethylene receptor mutant ein4 (right) lacks the triple response (left; see main text). (C) The triple cytokinin receptor mutant cre1 ahk2 ahk3 (right) shows reduced growth. (D) The root vascular bundle normally consists of xylem, phloem and procambium cell files, whereas in wol (bottom), or in cre1 ahk2 ahk3 (not shown), there are fewer vascular cell lineages, all of which differentiate as protoxylem. The vascular bundle is encircled by a layer of pericycle cells (asterisks) (E) The abscisic acid receptor mutant fca (right) flowers later than wild type, as demonstrated by increased leaf number at flowering. Scale bars: in C, 2 mm; in D, 10 µm. [A is reprinted, with permission, from Cano-Delgado et al. (Cano-Delgado et al., 2004); B is reprinted, with permission, from Hua et al. (Hua et al., 1998); E is reprinted, with permission, from Amasino (Amasino, 2003).]

View larger version (34K): [in a new window]   Fig. 6. Ethylene and cytokinin signalling pathways. (A) At low concentrations of the ligand, ethylene receptors are active and can therefore stimulate the negative regulator CTR1, which in turn shuts down ethylene signalling by allowing EIN3 degradation. (B) Ethylene binding inactivates the receptors and therefore they are unable to stimulate CTR1-mediated inhibition. As a result, EIN2 is active and prevents EIN3 degradation, which leads to EIN3 accumulation and activation of ethylene responsive gene transcription. (C) Cytokinin binding initiates autophosphorylation of the receptors, followed by transfer of the phosphoryl group (P) to a histidine phosphotransfer protein (AHP), and further on to a response regulator (ARR), which leads to the transcription of cytokinin-response genes. There may be some interaction between ethylene and cytokinin signalling through crosstalk via this phosphorelay. ER, endoplasmic reticulum; NM, nuclear membrane; PM, plasma membrane; +ub, ubiquitination.

View larger version (31K): [in a new window]   Fig. 7. The abscisic acid (ABA) signalling pathway that controls the regulation of flowering time. (A) At low ABA concentrations, FCA and FY interact and together prevent the accumulation of FLC mRNA. FLC is a potent inhibitor of flowering, as several pathways converge on it to block the expression of the floral integration gene SOC1 by directly binding to its promoter (Hepworth et al., 2002). (B) ABA binds to the C-terminal part of FCA, close to its interaction site with FY, disrupting the association of these two proteins in vitro and leading to the accumulation of FLC in vivo, which delays flowering. Transcription of SOC1 only occurs in plants with low FLC levels; additional cues are required for the transition to flowering.

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